Outline the effects of increasingly higher altitudes on the following factor:
partial pressure of oxygen in ambient air
Hyperventilation from reduced arterial Po2 is the most important immediate response, is an attempt to increase the partial pressure of O2. Hypoxic drive can remain elevated for a year.
Outline the effects of increasingly higher altitudes on the following factor: oxygen saturation of hemoglobin in pulmonary capillaries
Change in PV happens quickly and stimulates processes which turn on EPO to form new RBCs. After a week at 1300m, PV declines by 8%, RBC concentration increases by 4% and Hb by 10%. Rapid PV reduction and hemoconcentration incr the O2 content of arterial blood.
Outline the effects of increasingly higher altitudes on the following factor:
VO2max
Vo2max is reduced
Discuss the immediate physiological adjustments to exercise at high altitude:
- Hyperventilation, body fluids becoming more alkaline.
- incr. in submax HR and CO. SV and max CO remain same or slightly decr.
- incr. in respiration and BF
Discuss the longer-term physiological adjustments to exercise at high altitude
- Hyperventilation, excretion of bicarbonate via kidneys and reduction in alkaline reserve. Blood pH restored to normal level.
- Submax HR remains elevated, submax CO and SV decr, mac CO incr.
- Possible incr capillarization of skeletal muscle, aerobic enzymes and mitochondrial density, loss of BW and LBM.
Give symptoms, possible causes, and treatment for: Acute mountain sickness
- headache, nausea, dizziness, fatigue, insomnia, peripheral edema.
- From acute reduction in cerebral oxygen saturation, headache from hyperventilation.
- Slow altitude climb, oxygen and Diamox.
Give symptoms, possible causes, and treatment for: High altitude pulmonary edema
- severe headache and fatigue, excessively high VE and HR, mucus cough, blueish skin, disruption of bladder, vision and bowel, loss of reflexes and coordination, paralysis on one side.
- From rapid ascent, fluid accumulating in the brain and lungs, results from increased pulmonary artery pressure with damage to blood-gas barrier.
- Descent by at least 1000 m, oxygen, medication, hyperbaric chamber.
Give symptoms, possible causes, and treatment for: High altitude cerebral edema
- staggered gait, dyspnea, severe weakness/fatigue, cough with infection, confusion, impaired mental state, ashen skin color, LOC. - from increased intracranial pressure, cerebral vasodilation and elevations in capillary hydrostatic pressured moving fluid and protein from vascular compartment across blood brain barrier.
- Treat by immediately descending.
Describe the lactate paradox and possible causes
- On immediate ascent to altitude, a given submax exercise load increases BL concentration compared to SL values. Greater reliance on anaerobic metab w altitude hypoxia explains the increase in lactate accumulation.
- After a few weeks, the same intensity exercise produces lower BL levels despite a lack of incr in Vo2max or regional BF.
- Causes: reduced output of epinephrine, reduced glucose mobilization from the liver reducing capacity for lactate formation. Overall reduced CNS drive, reducing capacity for all out effort.
Summarize factors that affect the time course for altitude acclimatization
Depends on elevation, accl to one altitude ensures only partial adjustment to a higher elevation. After 2300 (two weeks) its an additional week per 610m altitude.
•Graph the relationship between increasing altitude exposure and the decrease in VO2max:
Altitude X, % decline in vo2max Y - straight down towards right.
Discuss alterations in circulatory function that offset the benefits of altitude acclimatization on oxygen transport capacity
After several months of acclimatization to hypoxia, Vo2max at altitude still remains below sea level values , despite incr in Hb concentration. Occurs because the reduced circulatory capacity (lowered max HR and SV) offsets benefits.
Discuss whether altitude training produces greater improvement than sea-level training on sea-level exercise performance.
does not improve after living at altitude when VO2max serves as improvement criterion. Any reduction in max CO from altitude exposure offsets benefits from an increase in the blood oxygen carrying capacity.
Describe the training concept of “live high train low.”:
Increase RBC count by eliciting benefits of both training at sea level and living at high altitude. Increase O2 transport by living at altitude, without detraining associated with hypoxic exercise.
Explain how the hypothalamus maintains thermal balance:
Hypothalamus contains the central coordinating center for temp regulation. Thermal receptors in the skin provide input to the central control center, and changes in the temp of blood that perfuses the hypothalamus directly stimulate this area.
Describe physical factors that contribute to heat loss and heat gain.
Conduction: warming air molecules and cooler surfaces that touch the skin.
Convection: transferring heat by notion of a gas or liquid across a heated surface. Air passes over skin and heat is exchanged w air molecules….
Radiation: all objects emit radiant energy or heat waves…
Evaporation: primary avenue for heat dissipation - liquid turns into gas. Three factors influence total amount of sweat vaporized from skin and pulmonary surfaces: surface exposed to env, temp and relative humidity of ambient air, convective air currents about the body.
Rate of conductive heat loss depends on two factors:
- temp gradient between the skin and the surrounding temperature, 2. the thermal qualities of the surface.
Discuss how the circulatory system adjusts during temperature changes:
- In heat, HR and CO incr while superficial and venous blood vessels dilate to divert warm blood to the skin.
- W/ extreme heat stress, 15-25% of CO passes thru the skin. Submax exercise produces a lower SV causing a higher HR at all submax intensities. Higher HR in max exercise does not offset SV decrease so max CO decreases.
- Maintaining skin and muscle BF requires other tissues to compromise blood supply. These circulatory adjustments lead to incr blood lactate accumulation due to; decr lactate uptake by live from reduced hepatic BF, less muscle catabolism of circulating lactate because heat dissipation diverts CO to the periphery.
Quantify fluid loss during hot-weather exercise
Peak of 3L per hour of intense PA, 12L on daily basis. Intense sweating for hours can produce sweat-gland fatigue that ultimately interferes w/ core temp regulation.
Discuss the purpose of fluid replacement and pre-exercise hydration.
- Maintaining fluid balance: must focus on maintain plasma volume so circulation and sweating progress normally.
- Ideal conditions replace water loss from sweating during exercise at a rate close or equal to sweating rate. Each lb of weight reps 450 ml dehydration.
- Hyperhydration before exercising in heat offers thermoregulatory protection: 500 ml of water before sleeping the night before, another 500 ml upon waking, and 400-600 ml 20 min before exercise.
Discuss factors that maintain cutaneous blood flow and blood pressure during exertion in heat.
- Compensatory restriction of the splanchnic vascular bed and renal tissues rapidly counteracts active vasodilation of the subcutaneous vessels responsible for 80-95% of elevated skin BF.
- Vasoconstriction in the viscera increases total vascular resistance. A balance between dilation and constriction maintains arterial BP during exercise in the heat. In intense effort, w/ accompanying dehydration, relatively less blood diverts to peripheral areas for heat dissipation. Reduced peripheral BF reflects the body’s attempt to maintain CO in the face of diminishing PV caused by sweating. circulatory regulation and muscle BF takes precedence over temp reg during PA in the head. When submax effort progresses without excessive physio strain, a greater dependence still exists on anaerobic metab.
Describe the cardiac output, heart rate, and stroke volume response during hot-weather physical activity.
Submax exercise produces a lower SV causing a higher HR at all submax intensities. Higher HR in max exercise does not offset SV decrease so max CO decreases
Explain how acclimatization, training, age, gender, and body fat modify heat tolerance during physical activity
- Acclimatization: Incr BF to cutaneous vessels, more effective CO, low sweating threshold, quicker cooling, incr sweat capacity , more diluted sweat (less salt lost)
- Training status: incr sensitivity and capacity of the sweat response to that sweating begins at a lower temp. Greater cutaneous BF at a given internal temp or % of vo2max.
- Age: no age related decrements in thermoreg during marathon running. Children sweat less and have higher core temps during heat stress.
- Gender: women sweat less and start to sweat at a higher skin and core temp, even after acclimatization. Likely make greater use of circulatory mechanisms for dissipating heat. Women are typically smaller and have a relatively larger body surface area per unit mass - favors greater heat dissipation.
- BF level: fat incr the insulatory capacity of the body shell and limits heat conduction to the periphery. Larger individuals have a smaller surface area to body mass ratio - limits the effectiveness of sweat evaporation.
Give symptoms, causes, and treatments for heat cramps, heat exhaustion, and heat stroke.
- Heat cramps: severe involuntary sustained and spreading muscle spasms during or after intense PA, usually in exercised muscle. Fatigue, excessive thirst, profuse sweating, cramps.
- Heat exhaustion: occurs from ineffective circulatory adjustments compounded by depletion of extracellular fluid, principally plasma volume, from excessive sweating. Nausea, chills, headache.
- Heat stroke: failure of heat regulating mechanisms from an excessively high core temp. Cessation of sweating, confusion, LOC.
